过热对脂多糖介导的大鼠急性肺损伤/急性呼吸窘迫综合征的影响

Aggravating effect of hyperthermia on lipopolysaccharide-mediated ALI/ARDS in rats

目的研究过热对脂多糖(LPS)介导的大鼠急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)的影响.方法雄性SPF级Wistar大鼠随机分为常温生理盐水组(C组),高温生理盐水组(H组),常温脂多糖组(L组),高温脂多糖组(HL组).持续描计动物直肠温度(Tr),并检测动物应激0,40,80,120min时血浆TNF-α,IL-6含量,动脉血气,血浆肺湿质量/干质量比值(W/D)以及肺病理改变.结果①HL组Tr上升到(43.04±0.11)℃,与C组,L组之间存在显著性差异(P<0.01),与H组之间不存在显著性差异(P>0.05);②HL组动物血浆TNF-α峰值(80min)及IL-6表达水平显著升高(P<0.01);③HL组HCO3-,PaCO2于致伤40min时即出现显著下降(P<0.01),致伤120min时分别为(10.42±1.06)mmol/L,(2.82±0.81)kPa;④HL组动物W/D显著性升高(P<0.05);肺急性微血管损伤有病理学改变.结论过热应激能够加重LPS介导的大鼠ALI/ARDS.

AIM： To observe the effect of hyperthermia on lipopolysaccharide （LPS）-mediated ALI/ARDS in rats. METHODS： Male specific-pathogen free Wistar rats were randomly assigned to the following groups： saline-injected normothermic control （C-Group）, saline-injected heat exposed （ H-Group）, LPS-injected normothermic control （ L- Group） and LPS-injected heat exposed （HL-Group）. Rectal temperature （Tr） was continually monitored. Plasma levels of TNF-α and IL-6, arterial blood gas, lung wet-to-dry weight ratio （W/D）, and lung histological change were observed at 0, 40, 80 and 120 min. RESULTS： ① The rats in HL-Group displayed significantly higher values of Tr （43.04±0.11 ） ℃ compared with C/L-Group （ P 〈0.01 ）. There was no significant difference between HL-Group and H- Group （ P 〉 0.05）. ② Significant elevations of the peak TNF-α level （at 80 min） and IL-6 expression were seen in HL-Group （ P〈0.01 ）. ③ The values of HCO3^- and PaCO2 significantly decreased at 40 min in HL-Group （ P 〈 0.01 ）. At 120 min, the values of HCO3^- and PaCO2 decreased to （ 10.42 ± 1.06） mmol/L and （2.82 ±0.81 ） kPa respectively. ④ Significantly increased W/D ratio and many pathological features of acute microvascular lung injury were seen in HL-Group. CONCLUSION： Hyperthermia may aggravate ALI/ARDS in LPS-injected rats.